Biochemical transition during triphasic postpartum thyroiditis: confusion with central hypothyroidism

Summary Hypothyroidism occurring in the postpartum period can be due to pituitary or hypothalamic disease as in Sheehan’s syndrome and postpartum autoimmune hypophysitis or due to a primary thyroid disease as in postpartum thyroiditis. It is important that the correct diagnosis is ascertained because hypothalamic or pituitary disorders are often associated with other pituitary hormone deficiencies, especially life-threatening adrenal insufficiency or adrenal crisis. A combination of various symptoms and biochemical markers, especially serum thyroid-stimulating hormone levels dictate the initial diagnostic pathway. We present a case of a woman who presented with a 2-month history of tiredness and neck discomfort following delivery. A thyroid function test demonstrated results, which we initially interpreted as central hypothyroidism. Follow-up results indicated that this was in fact the transition period between the thyrotoxic phase and hypothyroid phases of postpartum thyroiditis. This case highlights the potential for diagnostic confusion between central hypothyroidism and postpartum thyroiditis. Learning points Postpartum thyroiditis affects one in twenty mothers within 12 months of delivery. The majority of patients have transient thyrotoxicosis only, some have transient hypothyroidism only, and the rest has a triphasic pattern (thyrotoxic, hypothyroid then a euthyroid phase). During the transition from the thyrotoxic phase to hypothyroid phase, when serum TSH is still suppressed, the biochemical results can resemble that of central hypothyroidism. If central hypothyroidism is suspected, then urgent diagnostic investigations should be carried out along with the assessment of adrenal function. There is a potential for diagnostic confusion between postpartum central hypothyroidism and postpartum thyroiditis; however, the obstetric history, clinical symptoms, and signs (headaches, breastfeeding, goitre, etc.) and serum adrenocorticotropic levels should help with the differential diagnosis.

Postpartum Thyroiditis: A Case Report

ABSTRACT: Background: Postpartum thyroiditis (PPT) is a thyroid dysfunctionn syndrome which is temporary or permanent that occurs 1 year after giving birth or abortion. The occurrence of postpartum thyroiditis is 5 – 10% of postpartum women in the world. It is caused by an inflammation of the thyroid gland which leads to a destruction of the thyroid follicle and proteolysis of thyroglobulin. Case presentation: A woman, 31 years old, was admitted to the hospital complaining an enlargement on her neck. The patient said her the enlargement keeps getting larger and she also complained a feeling of something stuck in the throat. The patient also complained a hoarse voice. The patient has just given birth of her second child 5 months ago. From a hematologic examination, radiologic, and blood culture, the patient was diagnosed with Postpartum Thyroiditis. The patient was given Euthyrox therapy and will undergo repeated evaluation after 1 months of the therapy. Conclusion: We reported a case of Postpartum Thyroiditis that was treated comprehensively, and showed a good prognosis.

Postpartum Thyroid Abnormalities and Systemic Lupus Erythematosus: Is There a Link?

Introduction: Postpartum Thyroiditis (PPT) is an autoimmune disorder characterized by destruction of the thyroid gland within the first year after delivery. Systemic Lupus Erythematosus (SLE), another autoimmune disease, has been associated with a spectrum of thyroid disorders. While the prevalence of thyroid diseases in patients with SLE is increased, the association between SLE and PPT is not well known. The infrequency of encountering SLE and PPT makes abnormal thyroid tests in the postpartum period a diagnostic challenge. Clinical Case: A 27-year-old G1P1001 who was five months postpartum and not breast feeding was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests. Past medical history was significant for SLE with renal and pericardial involvement. SLE was well controlled, treated with hydroxychloroquine. Family history was significant for hypothyroidism in her mother. She was asymptomatic and appeared clinically euthyroid. Vitals were stable and physical exam was negative for goiter, nodule or orbitopathy. Lab results at two months postpartum showed an elevated TSH of 3.87 UIU/mL (Normal 0.40-3.8 UIU/mL) and at four months postpartum TSH was low at 0.012 UIU/mL. Repeat labs at five months postpartum continued to show a low TSH at 0.007 UIU/mL with mildly elevated Free T4 at 1.7 ng/dL (Normal 0.6-1.6 ng/dL) and elevated Free T3 of 6.0 pg/mL (Normal 2.1-3.8 pg/mL). Anti-thyroid peroxidase antibodies (TPO), thyroid stimulating antibodies (TSI) and TSH receptor antibodies (TRAb) were negative. Thyroid Ultrasound with Doppler was within normal limits. Radioactive Iodine Uptake and Scan, obtained at 6 months postpartum, showed high normal uptake (17% and 32% at 4 hours and 24 hours respectively), suggestive of recovery phase of PPT. The most recent TSH was elevated at 8.5 UIU/mL and Free T4 was low at 0.7 ng/dL. Disease course was consistent with PPT. Conclusion: The Th1 (T-helper) lymphocyte immune predominance in autoimmune thyroid disease and SLE is the immune-pathogenetic base of the association between both diseases. Postpartum thyroiditis is a variant of chronic autoimmune thyroiditis. Serum anti-TPO antibodies vary during pregnancy and tend to increase early and may decline later. Immunologic tolerance increases during pregnancy, fades in the postpartum period and makes interpretation of thyroid function tests and disease process challenging. Pregnant and postpartum patients who have SLE have increased prevalence of thyroid disease. Causes are multifactorial with a higher prevalence of hypothyroidism and thyroid autoantibodies. Hyperthyroidism is much less likely. One comparable study found 6 of 43 (14%) women with SLE developed PPT and only one of these patients had positive thyroid antibodies. These reports and our patient illustrate the variability of thyroid function tests in patients with SLE.

Thyroid Disease II: Hypothyroidism in Pregnancy

Hypothyroidism affects between 2 and 12 per 1000 pregnancies. Symptoms in pregnancy are similar those encountered in the nonpregnant population, but may be attributed to the pregnancy itself. Thyroxine-binding globulin increases in pregnancy, leading to increased thyroxine levels in order to meet the metabolic needs of normal pregnancy. Routine screening is not recommended, and testing should be done using a targeted approach in women with symptoms or history of thyroid disease. Diagnosis is based upon the finding of an elevated serum TSH using population and trimester-specific ranges. Overt hypothyroidism, identified by high serum TSH and low free thyroxine, is associated with increased risk of pregnancy-related complications, and is treated with maternal thyroxine supplementation. Adequate iodine is necessary for fetal neurodevelopment, and women with iodine deficiency may present with a goiter, though it is important to distinguish it from other causes of thyroid enlargement, including malignancy. Postpartum thyroiditis is diagnosed infrequently, as only a small subset of women will demonstrate the classic biphasic presentation, Additionally, symptoms are often vague, nonspecific, and self-limited. Importantly, many women are at risk of eventually developing permanent hypothyroidism. This review contains 6 tables, and 48 references. Key words: euthyroid, goiter, overt hypothyroidism, postpartum thyroiditis, thyroixine binding globulin, thyroid peroxidase, thryroid nodules